B cells, along with T cells, form the central adaptive response during viral infections. B cell response is highly specific, mounted by the virus-specific antibodies and other effector cytokines secreted by these cells. B cell activation can be follicular helper T (TFH) cell-dependent, or in some instances, independent of helper cells; both instances are prevalent in COVID-19 (Mathew et al., 2020). Under the influence of antigen-presenting dendritic cells, naïve CD4+ T cells differentiate into TFH cells, which are marked by high expressions of CXCR5 and IL-21, and low expressions of CCR7, IFN-γ, IL-4, and IL-17 (Rasheed et al., 2006; Nurieva et al., 2008; Morita et al., 2011). The activated TFH cells interact with B cells via CD40R-CD40L and other associated receptors to induce the production of antigen-specific antibodies in a well-coordinated and regulated process. This CD40R-CD40L interaction along with the secretion of IL-21 also allows the formation of long-lived memory B cells, while B cell-derived IL-6 and IL-27 help in reciprocal maintenance of TFH cells (Nurieva et al., 2008, 2009). A previous animal study has shown the essential role of these helper cells in mounting an adequate antibody response against SARS-CoV infection (Chen et al., 2010). The depletion of these cells was associated with a decline in antibody response and reduced viral clearance. Thus, virus-specific antibodies produced by B cells are critical for an effective immune response mounted by the host. These antibodies facilitate the clearance of the virus by either directly activating phagocytosis, opsonization, or activation of the antibody-dependent cellular cytotoxicity (ADCC) via effector NK cells. Cytokines released by the activation of innate and adaptive immune systems also activate the complement system. Viruses coated with the secreted antibodies from plasma cells eventually get eliminated by the complement system, reviewed by Risitano et al. (2020).